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Polystyrene microplastics arrest skeletal growth in puberty through accelerating osteoblast senescence

Environmental Pollution 2023 59 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 60 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Hao Chen Chun Pan, Chun Pan, Chun Pan, Chun Pan, Yujie Shi, Xiangyu Liu, Hao Chen Hao Chen Hao Chen Hao Chen Yujie Shi, Hao Chen Xinglong Wang, Yin Wu, Yu Shi, Hao Chen Chun Pan, Sihan Hu, Hao Chen Hao Chen Chun Pan, Chun Pan, Sihan Hu, Yujie Shi, Yujie Shi, Ke Li, Hao Chen Yujie Shi, Xiangyu Liu, Yu Shi, Chun Pan, Yin Wu, Hao Chen Hao Chen Hao Chen Chun Pan, Wenzheng Lin, Wenzheng Lin, Chun Pan, Zhuobin Xu, Xinglong Wang, Hao Chen Zhuobin Xu, Huihui Wang, Yujie Shi, Zhuobin Xu, Zhuobin Xu, Hao Chen Huihui Wang, Hao Chen

Summary

Researchers found that polystyrene microplastics accumulated in the bones of mice during puberty, leading to reduced body and bone length and impaired bone structure. The microplastics accelerated premature aging (senescence) of bone-building cells called osteoblasts, suppressing their ability to form new bone. The study suggests that microplastic exposure during critical growth periods may pose a risk to skeletal development.

Polymers
Body Systems
Models

Polystyrene microplastics (PS-MPs) have attracted worldwide attention to their massive accumulation in terrestrial and aquatic ecosystems. It has been demonstrated that MPs are easily to accumulate in organs and exert toxic effects. However, their exposure risk to the skeleton remains unknown. In this study, we observed PS-MPs accumulation in both the long bones and axial bones, leading to reduced body length, as well as femur and tibia length. PS-MPs treated mice exhibited redundant skeletal growth and impaired trabecular bone micro-architecture, which is due to the suppressed osteogenic ability as the number of osteoblasts decreased significantly in PS-MPs treated mice. In histological analysis, we observed the accumulation of senescent osteoblasts in the bone trabecula of PS-MPs treated mice, as well as the impaired autophagy with decreased autophagosome and reduced autophagy-related proteins in the senescent osteoblasts. Re-establishing autophagy effectively reversed the senescent phenotype in osteoblasts and ameliorated PS-MPs induced skeletal growth arrest. Hence, our study reveals the detrimental role of PS-MPs in skeletal growth in puberty through accelerating osteoblast senescence, which may be alleviated by reactivating the autophagy. This study provides new evidence of the PS-MPs on health threats and the potential therapeutic targets to reverse it.

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